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Pathogen research abs 1 || Pathogen research abs 2 || Pathogen research abs 3 || Pathogen research abs 4 || Pathogen research abs 5 || Hormone and endocrine research abs 1 || Hormone and endocrine research abs 2 || Hormone and endocrine research abs 3 || Hormone and endocrine research abs 4 || Hormone and endocrine research abs 5





J Cell Biochem. 2002;86(4):688-99.
Role of c-fos in the regulation of type X collagen gene expression by PTH and PTHrP: localization of a PTH/PTHrP-responsive region in the human COL10A1 enhancer.

Riemer S, Gebhard S, Beier F, Poschl E, von der Mark K.

Department of Experimental Medicine I, University of Erlangen-Nuremberg, Germany.

PTH and PTHrP have been shown to inhibit maturation of growth plate chondrocytes and the expression of type X collagen. In order to examine the regulatory mechanisms involved, fetal bovine growth plate chondrocytes were incubated for 24-48 h under serum-free conditions with PTH and PTHrP and various aminoterminal, midregional, and carboxyterminal fragments of these hormones. Analysis of type X collagen mRNA levels by Northern hybridization showed a significant suppression by PTH (1-84), PTH (1-34), and PTHrP (1-40), but not by PTH (28-48) or PTH (53-84). PTH fragment (3-34) did not reduce alpha1(X) mRNA levels, while bis-indolylmaleimide, an inhibitor of the protein-kinase C pathway, did not affect alpha1(X) mRNA suppression by PTH, supporting the notion that the inhibition of type X collagen expression by PTH involves predominantly the adenylate cyclase pathway of the PTH/PTHrP-receptor. Since PTH and PTHrP have been shown to induce c-fos in osteoblasts and chondrocytes, the possibility was tested that c-fos mediated the suppressive effect of PTH/PTHrP on collagen X expression. In fetal bovine hypertrophic chondrocytes PTH (1-34), but not PTH (3-34) nor the midregional or C-terminal PTH fragments induced c-fos expression. In order to identify cis- and trans-acting elements in the COL10A1 gene involved in c-fos-mediated inhibition of collagen X expression by PTH/PTHrP, reporter gene constructs carrying various fragments of the human COL10A1 promoter coupled to the luciferase gene were transfected into hypertrophic chondrocytes. A tissue-specific, strong enhancer region, which we had previously located in the promoter of the human type X collagen gene COL10A1, was further narrowed down to a 530-bp sequence, located between - 1,870- and - 2,407 bp upstream of the transcription start site. The transcriptional activity of this enhancer element in transfected hypertrophic chondrocytes was significantly reduced after incubation with PTH (1-34) or PTHrP (1-40). Transcription of these reporter genes was also inhibited when chondrocytes were cotransfected with a c-fos expression vector. These results indicate the presence of a PTH/PTHrP responsive element in the human COL10A1 enhancer, which may be represented by multiple putative AP-1 sites located in this region. 2002 Wiley-Liss, Inc.


online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12210735&dopt=Abstract



J Cell Biochem. 2002;86(4):773-83.
Involvement of PI3-kinase and its association with c-Src in PTH-stimulated rat enterocytes.

Gentili C, Morelli S, Russo De Boland A.

Departamento de Biologia, Bioquimica & Farmacia, Universidad Nacional del Sur. Bahia Blanca 8000, Argentina.

Phosphoinositide-3-kinase (PI3K) is a lipid kinase, which phosphorylates the D3 position of phosphoinositides, and is known to be activated by a host of protein tyrosine kinases. PI3K plays an important role in mitogenesis in several cell systems. However, whether parathyroid hormone (PTH) affects the activity and functional roles of PI3K in intestinal cells remain to be determined. The objective of this study was to identify and characterize the PI3K pathway, and its relation to other non-receptor tyrosine kinases in mediating PTH signal transduction in rat enterocytes. PTH dose- and time-dependently increased PI3K activity with a peak occurring at 2 min. The tyrosine kinase inhibitor genistein, c-Src inhibitor PP1 and two structurally different inhibitors of PI3K, LY294002 and wortmannin, suppressed PI3K activity dependent on PTH. Co-immunoprecipitation analysis showed a constitutive association between c-Src and PI3K, which was enhanced by PTH treatment, suggesting that the cytosolic tyrosine kinase forms an immunocomplex with PI3K probably via the N-SH2 domain of the p85alpha regulatory subunit. In response to PTH, tyrosine phosphorylation of p85alpha was enhanced, effect that was abolished by PP1, the inhibitor of c-Src kinase. PTH causes a rapid (0.5-5 min) phosphorylation of Akt/PKB, effect that was abrogated by PI3K inhibitors, indicating that in rat enterocytes, PI3K is an upstream mediator of Akt/PKB activation by PTH. We report here that PI3K is also required for PTH activation of the mitogen-activated protein kinases ERK1 and ERK2. Taken together, the present study demonstrate, for the first time, that PTH rapidly and transiently stimulates PI3K activity and its down effector Akt/PKB in rat enterocytes playing c-Src kinase a central role in PTH-dependent PI3K activation and that PI3K signaling pathway contributes to PTH-mediated MAPK activation. 2002 Wiley-Liss, Inc.


online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12210743&dopt=Abstract



Mol Cell Endocrinol. 1999 Jan 25;147(1-2):149-59.
Growth hormone and the expression of mRNAs for matrix proteins and oncogenes in bone.

Salih MA, Orhii PB, Chen C, Kalu DN.

Department of Physiology, University of Texas Health Science Center at San Antonio, 78284-7756, USA.

To examine the effects of growth hormone (GH) on the expression of the mRNAs of bone matrix proteins, three experiments were carried out with 3-month-old female Sprague-Dawley rats. In the first experiment rats were given a single subcutaneous injection of recombinant human GH (8 mg rhGH/kg b. wt.), sacrificed 15 min, 1 h, 2 h, 4 h, 8 h, 16 h and 24 h later, and RNA isolated from cancellous bone from the distal femoral metaphysis. Growth hormone increased the level of type I collagen mRNA by 187, 417, and 509% over the control level at 15 min, 1 h and 2 h, respectively; the mRNA levels declined to 119 and 99% at 4 and 8 h, respectively, and then rose again to 351 and 423% over the control level at 16 and 24 h, respectively. Osteocalcin mRNA transcript increased by 89, 90, 325, 342, 361, and 407% over the control level at 15 min, 1 h, 2 h, 4 h, 8 h and 16 h, respectively, and fell to 66% at 24 h. The level of IGF-I mRNA increased by 45, 83, 120, 140, and 175% over the control level at 2, 4, 8, 16, and 24 h, respectively. In the second experiment, following the administration of rhGH (8 mg/kg b. wt.) bone osteocalcin mRNA increased by 127, 177, 361, and 413% over the control level at 30 min, 1 h, 2 h and 4 h, respectively; IGF-I mRNAs increased by 38, 33, 87, and 437 at 30 min, 1 h, 2 h and 4 h, respectively, but the levels did not become significant until 2 h; c-fos mRNA increased significantly at 30 min, and c-jun and c-myc mRNAs did not increase until 4 h. In the third experiment, animals were given a single injection of rhGH (8 mg/kg b. wt.) and the animals were bled at timed intervals and acid ethanol-extractable serum IGF-I determined. Serum IGF-I increased significantly only at 12 h following rhGH administration. Our data indicate that GH stimulates a rapid increase in the expression of mRNAs for the bone matrix proteins, type I collagen and osteocalcin, by a mechanism that appears to be independent of IGF-I, the early response oncogenes or an increase in osteoblast number.


online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=10195702&dopt=Abstract



J Cell Biochem. 2002;86(3):601-12.
Differential nuclear receptor signalling from DR4-type response elements.

Quack M, Frank C, Carlberg C.

Institute for Physiological Chemistry I, Heinrich-Heine-University, D-40001 Dusseldorf, Germany.

Nuclear receptors form a large family of highly related transcription factors that transform an incoming signal in the form of a lipophilic hormone into an activation of the basal transcriptional machinery. The specific recognition of nuclear receptor DNA binding sites, referred to as response elements (REs), determines the genes that can be regulated by nuclear hormones. In this study, it was shown that the complexes of the retinoid X receptor (RXR) with either the vitamin D3 receptor (VDR), the thyroid hormone receptor (T3R) or the liver X receptor (LXR) have comparable functionality on a RE of the rat pit-1 gene that is formed by a direct repeat of two hexameric binding motifs spaced by 4 nucleotides (DR4). The sequence of two nucleotides 5'-flanking the downstream binding motif of this DR4-type RE and, interestingly, also those flanking the upstream motif were shown to have in part rather drastic and receptor-specific effects on heterodimer complex formation on DNA. In particular, a downstream substitution into GA reduced the complex formation for LXR specifically, while upstream substitutions into AA or TA increase complex formation for LXR and, to a lesser extent, T3R. The preference of this in vitro complex formation was shown to correlate well with the functional activity of the nuclear receptors in living cells. The results of this study allow (i) a more detailed understanding of known REs, (ii) a more straightforward search for putative REs in newly identified promoter sequences, for example, of the whole human genome, and (iii) a more precise prediction of the hormone responsiveness of the respective genes. 2002 Wiley-Liss, Inc.


online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12210766&dopt=Abstract



Mol Reprod Dev. 2002 Sep;63(1):24-31.
Structure and expression of the follicle-stimulating hormone receptor gene in a marsupial, Macropus eugenii.

Mattiske D, Pask AJ, Shaw JM, Shaw G.

Department of Zoology, University of Melbourne, Australia. d.mattiskoology.unimelb.edu.au

Follicle stimulating hormone (FSH) is essential for folliculogenesis. The function of FSH is mediated through its receptor (FSHr) and modulation of the receptor is thought to be the mechanism by which the responsiveness of follicles to gonadotrophins is regulated. FSHr is alternatively spliced to produce several transcripts in all eutherian species studied. However, controversy exists over the significance of alternatively spliced transcripts. In this study, we cloned and characterised the tammar wallaby (Macropus eugenii) FSHr gene and examined its expression. Comparison of gene structure and function between marsupials and eutherians enables identification of conserved features that are likely to be of functional significance. Tammar FSHr shares 94% amino acid similarity with human FSHr and is expressed in both the adult testis and ovary suggesting a similar function for this gene in both marsupials and eutherians. Tammar FSHr undergoes alternate splicing to produce four transcripts consistent with the splice variants seen in eutherians. These results strongly suggest that alternate splicing is of functional significance in the ovary since it has remained a highly conserved character of this gene for over 100 million years of divergent evolution. 2002 Wiley-Liss, Inc.


online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12211057&dopt=Abstract







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